Cytogenetic damage in human lymphocytes following GMSK phase modulated microwave exposure
Cytogenetic damage in human lymphocytes following GMSK phase modulated microwave exposure
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DOI：
10.1002/bem.93
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发表时间：
2002-01-01
影响因子：
1.9
通讯作者：
Zeni, O
中科院分区：
文献类型：
--
作者：
d'Ambrosio, G;Massa, R;Zeni, O
本研究使用人体淋巴细胞体外实验，通过评价胞质分裂阻滞增殖指数和微核频率，研究暴露于用于移动的通信的微波频率（未调制或仅存在相位调制）是否会导致细胞增殖动力学改变和/或遗传毒性效应。在GSM 1800移动的通信系统中，场是相位（高斯最小频移键控，GMSK）和幅度（时域多址，TDMA）调制的。本研究仅研究了相位调制的影响，而没有应用幅度调制。将人外周血培养物暴露于1.748 GHz的连续波（CW）或纯相位调制波（GMSK）15 min。最大比吸收率（类似于5 W/kg）高于移动的手机用户头部的最大比吸收率;然而，暴露于CW或GMSK场后，细胞增殖动力学没有发现变化。就遗传毒性而言，微核频率结果不受CW暴露的影响;然而，在暴露于相位调制场后发现了统计学显著的微核效应。这些结果表明相位调制本身具有遗传毒性。Bioelectromagnetics 23：7-13，2002. (C)2002 Wiley-Liss，Inc.
The present study investigated, using in vitro experiments on human lymphocytes, whether exposure to a microwave frequency used for mobile communication, either unmodulated or in presence of phase only modulation, can cause modification of cell proliferation kinetics and/or genotoxic effects, by evaluating the cytokinesis block proliferation index and the micronucleus frequency. In the GSM 1800 mobile communication systems the field is both phase (Gaussian minimum shift keying, GMSK) and amplitude (time domain multiple access, TDMA) modulated. The present study investigated only the effects of phase modulation, and no amplitude modulation was applied. Human peripheral blood cultures were exposed to 1.748 GHz, either continuous wave (CW) or phase only modulated wave (GMSK), for 15 min. The maximum specific absorption rate (similar to5 W/kg) was higher than that occurring in the head of mobile phone users; however, no changes were found in cell proliferation kinetics after exposure to either CW or GMSK fields. As far as genotoxicity is concerned, the micronucleus frequency result was not affected by CW exposure; however, a statistically significant micronucleus effect was found following exposure to phase modulated field. These results would suggest a genotoxic power of the phase modulation per se. Bioelectromagnetics 23:7-13, 2002. (C) 2002 Wiley-Liss, Inc.